أسئلة ضع دائرة على السكري Flashcards

(233 cards)

1
Q

Which hormone is produced by β cells in the pancreas?
a. Glucagon
b. Somatostatin
c. Insulin
d. Amylin

A

c. Insulin

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2
Q

Which cells in the pancreas are responsible for producing glucagon?
a. β cells
b. α cells
c. δ cells
d. PP cells

A

b. α cells

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3
Q

Somatostatin is produced by which type of cells in the pancreas?
a. β cells
b. α cells
c. δ cells
d. PP cells

A

c. δ cells

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4
Q

What condition is caused by a lack of insulin?
a. Hypoglycemia
b. Severe hyperglycemia
c. Hyperthyroidism
d. Hypothyroidism

A

b. Severe hyperglycemia

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5
Q

Untreated severe hyperglycemia can lead to which of the following complications?
a. Retinopathy
b. Nephropathy
c. Neuropathy
d. All of the above

A

d. All of the above

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6
Q

How many people worldwide are affected by diabetes?
a. 100 million
b. 150 million
c. 180 million
d. 200 million

A

c. 180 million

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7
Q

Diabetes is best described as:
a. A single disease
b. A group of heterogeneous syndromes
c. A viral infection
d. A bacterial infection

A

b. A group of heterogeneous syndromes

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8
Q

Which of the following is NOT a clinical classification of diabetes?
a. Type 3: insulin-resistant
b. Type 1: insulin-dependent
c. Type 2: non-insulin-dependent
d. Gestational diabetes

A

a. Type 3: insulin-resistant

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9
Q

Gestational diabetes affects which group of people?
a. Elderly
b. Teenagers
c. Pregnant women
d. Infants

A

c. Pregnant women

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10
Q

Diabetes due to other factors can be caused by:
a. Viral infections
b. Genetics or medication
c. Poor diet
d. Lack of exercise

A

b. Genetics or medication

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11
Q

Type 1 diabetes most commonly affects individuals in:
a. Infancy
b. Puberty or early adulthood
c. Middle age
d. Old age

A

b. Puberty or early adulthood

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12
Q

What is the cause of absolute insulin deficiency in type 1 diabetes?
a. Insulin resistance
b. Massive β-cell necrosis
c. Decreased insulin production
d. Increased glucagon production

A

b. Massive β-cell necrosis

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13
Q

The autoimmune process in type 1 diabetes is directed against which cells?
a. α cells
b. δ cells
c. β cells
d. PP cells

A

c. β cells

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14
Q

Which of the following are symptoms of type 1 diabetes?
a. Polydipsia, polyuria, and weight loss
b. Hyperactivity, weight gain, and hypertension
c. Hypoglycemia, fatigue, and muscle cramps
d. Fever, chills, and headaches

A

a. Polydipsia, polyuria, and weight loss

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15
Q

What life-threatening condition is associated with type 1 diabetes?
a. Hyperglycemic hyperosmolar syndrome
b. Ketoacidosis
c. Hypoglycemia
d. Diabetic foot

A

b. Ketoacidosis

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16
Q

To control hyperglycemia and ketoacidosis in type 1 diabetes, what is required?
a. Oral hypoglycemic agents
b. Exogenous insulin
c. Dietary modifications only
d. Exercise only

A

b. Exogenous insulin

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17
Q

Maintaining the accepted level of glycosylated hemoglobin (HbA1c) helps to avoid:
a. Hypoglycemia
b. Hyperthyroidism
c. Long term complications
d. Hypertension

A

c. Long term complications

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18
Q

Individuals with type 1 diabetes cannot maintain normal levels of which hormone?
a. Glucagon
b. Somatostatin
c. Insulin
d. Cortisol

A

c. Insulin

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19
Q

What type of diabetes is most common?
a. Type 2
b. Type 1
c. Gestational diabetes
d. MODY (Maturity Onset Diabetes of the Young)

A

a. Type 2

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20
Q

Which factors influence the development of type 2 diabetes?
a. Viral infections
b. Genetic factors, aging, obesity, and peripheral insulin resistance
c. Lack of physical activity
d. Excessive sugar intake

A

b. Genetic factors, aging, obesity, and peripheral insulin resistance

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21
Q

Type 2 diabetes is characterized by:
a. Severe metabolic alterations
b. Milder metabolic alterations than type 1
c. Ketoacidosis
d. Complete loss of β-cell function

A

b. Milder metabolic alterations than type 1

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22
Q

In type 2 diabetes, what happens to β-cell function over time?
a. It remains constant
b. It improves
c. It declines
d. It completely stops

A

c. It declines

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23
Q

What is the major cause of type 2 diabetes?
a. Excessive insulin production
b. Lack of sensitivity of target organs to insulin
c. Autoimmune destruction of β-cells
d. Increased glucagon production

A

b. Lack of sensitivity of target organs to insulin

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24
Q

Which of the following is NOT a characteristic of type 2 diabetes?
a. Ketoacidosis
b. Retention of some β-cell function
c. Variable insulin secretion
d. Gradual reduction in β-cell mass

A

a. Ketoacidosis

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25
The treatment for type 2 diabetes primarily aims to: a. Increase insulin production b. Induce weight loss c. Prevent long-term complications d. Enhance glucose absorption
c. Prevent long-term complications
26
As type 2 diabetes progresses, what is often required to maintain satisfactory serum glucose levels? a. Increased physical activity b. Insulin therapy c. Reduced carbohydrate intake d. Increased protein intake
b. Insulin therapy
27
Why is insulin administered by subcutaneous injection? a. It is degraded in the GIT if taken orally b. It is more effective when injected c. It causes less pain d. It has a longer duration of action
a. It is degraded in the GIT if taken orally
28
Insulin is synthesized as which precursor? a. Pre-insulin b. Pro-insulin c. Pre-pro-insulin d. Insulinogen
b. Pro-insulin
29
The process that converts pro-insulin to insulin involves: a. Proteolytic cleavage b. Hydrolysis c. Oxidation d. Phosphorylation
a. Proteolytic cleavage
30
Which cells secrete insulin and C peptide? a. α cells b. δ cells c. β cells d. PP cells
c. β cells
31
Measurement of which peptide provides a better index of insulin levels? a. Insulin b. C peptide c. Glucagon d. Amylin
b. C peptide
32
What is the most important regulator of insulin secretion? a. Blood glucose b. Certain amino acids c. Gastrointestinal hormones d. Autonomic mediators
a. Blood glucose
33
Which of the following also regulates insulin secretion? a. Blood pressure b. Blood pH c. Certain amino acids d. Blood oxygen levels
c. Certain amino acids
34
Insulin secretion is influenced by gastrointestinal hormones and: a. Blood cholesterol b. Autonomic mediators c. Plasma proteins d. Blood calcium levels
b. Autonomic mediators
35
What enzyme phosphorylates glucose in the pancreas? a. Hexokinase b. Glucokinase c. Phosphofructokinase d. Glucose-6-phosphatase
b. Glucokinase
36
The phosphorylation of glucose in the pancreas leads to the production of: a. ADP b. AMP c. ATP d. GTP
c. ATP
37
ATP production in the pancreas inhibits the efflux of which ion? a. Sodium (Na+) b. Potassium (K+) c. Calcium (Ca++) d. Chloride (Cl-)
b. Potassium (K+)
38
The inhibition of K+ efflux causes what cellular event? a. Hyperpolarization b. Depolarization c. Repolarization d. Hypopolarization
b. Depolarization
39
The increased intracellular concentration of which ion stimulates insulin secretion? a. Sodium (Na+) b. Calcium (Ca++) c. Potassium (K+) d. Chloride (Cl-)
b. Calcium (Ca++)
40
Which process results in the direct secretion of insulin? a. Inhibition of ATP production b. Hyperpolarization of pancreatic cells c. Decreased intracellular calcium levels d. Depolarization of pancreatic cells leading to increased intracellular calcium levels
d. Depolarization of pancreatic cells leading to increased intracellular calcium levels
41
The variation in the times of onset and durations of activity of insulin preparations is primarily due to: a. Differences in the amino acid sequences of the polypeptides and the type of formulation b. The source of insulin c. The dosage of insulin d. The route of administration
a. Differences in the amino acid sequences of the polypeptides and the type of formulation
42
Which of the following insulins have a faster onset and shorter duration of action than regular insulin? a. Glargine and detemir b. Lispro, aspart, and glulisine c. NPH and regular insulin d. Lente and ultralente
b. Lispro, aspart, and glulisine
43
Why do insulins like lispro, aspart, and glulisine have a faster onset of action? a. They are administered orally b. They are more potent c. They do not aggregate or form complexes d. They have a higher concentration
c. They do not aggregate or form complexes
44
Which insulins are classified as long-acting and show prolonged, flat levels of the hormone following injection? a. Glargine and detemir b. Lispro and aspart c. Regular and NPH d. Lente and ultralente
a. Glargine and detemir
45
What characteristic of glargine and detemir makes them suitable as long-acting insulins? a. They are rapidly absorbed b. They have prolonged, flat levels of the hormone c. They are taken orally d. They are mixed with other insulins
b. They have prolonged, flat levels of the hormone
46
What is the most serious and common adverse reaction to an overdose of insulin? a. Weight gain b. Lipodystrophy c. Hypoglycemia d. Allergic reactions
c. Hypoglycemia
47
Which of the following is a possible adverse reaction to insulin? a. Hair loss b. Muscle cramps c. Weight gain d. Hyperglycemia
c. Weight gain
48
Which adverse reaction to insulin is less common with human insulin? a. Hypoglycemia b. Lipodystrophy c. Weight gain d. Allergic reactions
b. Lipodystrophy
49
Adverse reactions to insulin can include: a. Allergic reactions and local injection site reactions b. Increased appetite and sweating c. Dehydration and dry skin d. Fever and chills
a. Allergic reactions and local injection site reactions
50
Hypoglycemia caused by an insulin overdose is considered: a. Mild and rare b. The most serious and common adverse reaction c. Temporary and harmless d. Unrelated to insulin dosage
b. The most serious and common adverse reaction
51
Which of the following is a type of rapid-acting insulin preparation? a. Insulin glargine b. Insulin lispro c. NPH insulin d. Insulin detemir
b. Insulin lispro
52
Which insulin can be given intravenously in emergencies? a. Regular insulin b. Insulin aspart c. Insulin glulisine d. Insulin lispro
a. Regular insulin
53
What is the pregnancy category for rapid-acting and short-acting insulin preparations? a. Category B b. Category A c. Category C d. Category D
a. Category B
54
Rapid-acting insulin preparations are usually administered: a. Once a day in the morning b. At bedtime c. Immediately before or following a meal d. Once a week
c. Immediately before or following a meal
55
Why are rapid-acting insulins like lispro, aspart, and glulisine used? a. To replace basal insulin b. To mimic the prandial (mealtime) release of insulin c. To treat diabetic ketoacidosis d. To manage long-term glucose control
b. To mimic the prandial (mealtime) release of insulin
56
What is the primary action of rapid-acting insulin preparations? a. Rapidly lowers blood glucose b. Slowly decreases blood glucose c. Increases blood glucose d. Stabilizes blood glucose levels
a. Rapidly lowers blood glucose
57
Rapid-acting insulin preparations are often used in combination with: a. Oral hypoglycemic agents b. Longer-acting insulins c. Dietary supplements d. Exercise regimens
b. Longer-acting insulins
58
What characteristic allows insulin lispro to act more rapidly after subcutaneous injection compared to regular insulin? a. Higher potency b. More rapid absorption c. Longer duration of action d. Delayed onset of action
b. More rapid absorption
59
What is another name for Neutral Protamine Hagedorn (NPH) insulin? a. Insulin lispro b. Insulin glulisine c. Insulin glargine d. Insulin isophane
d. Insulin isophane
60
NPH insulin should only be given: a. Intravenously b. Subcutaneously c. Orally d. Intramuscularly
b. Subcutaneously
61
NPH insulin is classified as: a. Rapid-acting insulin b. Short-acting insulin c. Intermediate-acting insulin d. Long-acting insulin
c. Intermediate-acting insulin
62
NPH insulin forms a less-soluble complex due to the presence of: a. Zinc b. Protamine c. Albumin d. Phosphate
b. Protamine
63
The delayed absorption of NPH insulin is caused by: a. Increased solubility b. Rapid metabolism c. Formation of a less-soluble complex d. Higher concentration of insulin
c. Formation of a less-soluble complex
64
The duration of action of NPH insulin is considered: a. Short b. Intermediate c. Long d. Ultra-long
b. Intermediate
65
What pH level does NPH insulin have? a. Acidic b. Basic c. Neutral d. Alkaline
c. Neutral
66
Which of the following statements about NPH insulin is true? a. It can be given intravenously in emergencies b. It is rapidly absorbed c. It should never be given intravenously d. It is a long-acting insulin
c. It should never be given intravenously
67
Intermediate-acting insulin is useful in treating all forms of diabetes except: a. Type 1 diabetes b. Type 2 diabetes c. Diabetic ketoacidosis or emergency hyperglycemia d. Gestational diabetes
c. Diabetic ketoacidosis or emergency hyperglycemia
68
Intermediate-acting insulin is usually given along with: a. Long-acting insulin b. Oral hypoglycemic agents c. Rapid- or short-acting insulin d. Dietary supplements
c. Rapid- or short-acting insulin
69
What is the role of intermediate-acting insulin in diabetes management? a. To treat hypoglycemia b. To provide basal insulin coverage c. To manage acute hyperglycemia d. To replace rapid-acting insulin
b. To provide basal insulin coverage
70
Neutral protamine lispro (NPL) insulin is used only in combination with: a. Insulin glargine b. Insulin detemir c. Insulin lispro d. Regular insulin
c. Insulin lispro
71
Which of the following is a premixed combination of human insulins? a. 100% NPH insulin b. 70% NPH insulin plus 30% regular insulin c. 50% NPH insulin plus 50% insulin glulisine d. 75% insulin glargine plus 25% insulin lispro
b. 70% NPH insulin plus 30% regular insulin
72
What is the purpose of using premixed combinations of human insulins? a. To treat diabetic ketoacidosis b. To provide both basal and prandial insulin coverage c. To manage insulin resistance d. To reduce insulin dosage
b. To provide both basal and prandial insulin coverage
73
What is the isoelectric point of insulin glargine compared to human insulin? a. Higher b. Lower c. The same d. Variable
b. Lower
74
The lower isoelectric point of insulin glargine leads to what at the injection site? a. Precipitation, thereby extending its action b. Rapid absorption c. Immediate release d. Decreased efficacy
a. Precipitation, thereby extending its action
75
Compared to NPH insulin, insulin glargine has a: a. Faster onset b. Slower onset c. Similar onset d. Variable onset
b. Slower onset
76
Insulin glargine is characterized by: a. A rapid peak b. No peak (flat) c. Multiple peaks d. Irregular peaks
b. No peak (flat)
77
Insulin glargine must be administered: a. Orally b. Intravenously c. Intramuscularly d. Subcutaneously
d. Subcutaneously
78
What type of hypoglycemic effect is associated with insulin glargine? a. Short-acting b. Prolonged hypoglycemic c. Immediate d. Variable
b. Prolonged hypoglycemic
79
Insulin glargine's action is extended due to: a. Increased solubility b. Precipitation at the injection site c. Rapid metabolism d. Increased dosage
b. Precipitation at the injection site
80
The administration route of insulin glargine is primarily: a. Oral b. Intravenous c. Subcutaneous d. Intramuscular
c. Subcutaneous
81
Insulin detemir has a fatty-acid side chain that enhances its association with which protein? a. Hemoglobin b. Myoglobin c. Albumin d. Fibrinogen
c. Albumin
82
The slow dissociation from albumin results in which property of insulin detemir? a. Rapid-acting b. Long-acting c. Intermediate-acting d. Short-acting
b. Long-acting
83
Which insulin has similar long-acting properties to insulin detemir due to its slow dissociation from albumin? a. Insulin lispro b. Insulin aspart c. Insulin glulisine d. Insulin glargine
d. Insulin glargine
84
The enhanced association of insulin detemir with albumin is due to: a. Increased solubility b. Higher concentration c. Fatty-acid side chain d. Protein binding
c. Fatty-acid side chain
85
Which characteristic of insulin detemir allows it to have prolonged effects similar to insulin glargine? a. Rapid absorption b. Immediate release c. Slow dissociation from albumin d. High potency
c. Slow dissociation from albumin
86
Insulin detemir is classified as which type of insulin preparation? a. Rapid-acting b. Short-acting c. Long-acting d. Intermediate-acting
c. Long-acting
87
The fatty-acid side chain in insulin detemir contributes to: a. Faster onset of action b. Reduced potency c. Enhanced association with albumin d. Increased degradation
c. Enhanced association with albumin
88
The prolonged action of insulin detemir is mainly due to: a. Slow dissociation from albumin b. Fast absorption c. High dosage d. Rapid metabolism
a. Slow dissociation from albumin
89
Pramlintide is a synthetic analog of: a. Amylin b. Insulin c. Glucagon d. Somatostatin
a. Amylin
90
Pramlintide is indicated as an adjunct to which type of insulin therapy? a. Basal insulin therapy b. Mealtime insulin therapy c. Long-acting insulin therapy d. Intermediate-acting insulin therapy
b. Mealtime insulin therapy
91
Which of the following is an effect of pramlintide? a. Increases gastric emptying b. Delays gastric emptying c. Increases postprandial glucagon secretion d. Decreases insulin sensitivity
b. Delays gastric emptying
92
Pramlintide helps to decrease which of the following? a. Insulin production b. Postprandial glucagon secretion c. Blood pressure d. Cholesterol levels
b. Postprandial glucagon secretion
93
How is pramlintide administered? a. Orally b. Intravenously c. Intramuscularly d. Subcutaneously
d. Subcutaneously
94
When should pramlintide be injected? a. Once a day in the morning b. At bedtime c. Immediately after meals d. Immediately prior to meals
d. Immediately prior to meals
95
Pramlintide is used in the management of which types of diabetes? a. Type 1 diabetes only b. Type 2 diabetes only c. Both Type 1 and Type 2 diabetes d. Gestational diabetes
c. Both Type 1 and Type 2 diabetes
96
Which of the following statements is true about pramlintide? a. It increases postprandial glucagon secretion b. It is administered intravenously c. It delays gastric emptying d. It is not indicated for use with mealtime insulin
c. It delays gastric emptying
97
When initiating pramlintide, the dose of rapid- or short-acting insulin should be decreased by: a. 25% b. 50% c. 75% d. 100%
b. 50%
98
Why should the dose of rapid- or short-acting insulin be decreased when starting pramlintide? a. To avoid a risk of severe hypoglycemia b. To increase insulin effectiveness c. To prevent hyperglycemia d. To reduce gastrointestinal side effects
a. To avoid a risk of severe hypoglycemia
99
The adverse effects of pramlintide are mainly: a. Neurological b. Cardiovascular c. Gastrointestinal d. Respiratory
c. Gastrointestinal
100
Which of the following is NOT a common adverse effect of pramlintide? a. Nausea b. Anorexia c. Hyperglycemia d. Vomiting
c. Hyperglycemia
101
Pramlintide should not be given to patients with: a. Hypertension b. Hyperlipidemia c. Diabetic gastroparesis d. Osteoporosis
c. Diabetic gastroparesis
102
Pramlintide should be avoided in patients with a history of: a. Hyperglycemia b. Hypothyroidism c. Hypoglycemic unawareness d. Hypercalcemia
c. Hypoglycemic unawareness
103
The main reason for avoiding pramlintide in patients with diabetic gastroparesis is: a. Increased blood pressure b. Delayed stomach emptying c. Increased insulin secretion d. Decreased insulin sensitivity
b. Delayed stomach emptying
104
Pramlintide is administered to manage which condition? a. Hypertension b. Hyperlipidemia c. Diabetes d. Osteoporosis
c. Diabetes
105
Sulfonylureas promote the release of insulin from which cells of the pancreas? a. α cells b. β cells c. δ cells d. PP cells
b. β cells
106
What is one of the mechanisms of action of sulfonylureas? a. Inhibition of insulin release b. Stimulation of insulin release by blocking ATP-sensitive K+ channels c. Decrease in peripheral insulin sensitivity d. Increase in hepatic glucose production
b. Stimulation of insulin release by blocking ATP-sensitive K+ channels
107
Blocking ATP-sensitive K+ channels by sulfonylureas leads to: a. Hyperpolarization b. Depolarization and Ca2+ influx c. Decreased calcium levels d. Reduced insulin secretion
b. Depolarization and Ca2+ influx
108
Sulfonylureas may cause which of the following side effects? a. Hyperglycemia b. Hypoglycemia c. Hyperkalemia d. Hypokalemia
b. Hypoglycemia
109
Which of the following is an additional action of sulfonylureas? a. Increase in hepatic glucose production b. Reduction in hepatic glucose production c. Increase in insulin degradation d. Inhibition of gluconeogenesis
b. Reduction in hepatic glucose production
110
Sulfonylureas also contribute to diabetes management by: a. Decreasing insulin sensitivity b. Inhibiting insulin receptors c. Increasing peripheral insulin sensitivity d. Reducing glucose uptake
c. Increasing peripheral insulin sensitivity
111
What is the result of increased peripheral insulin sensitivity due to sulfonylureas? a. Enhanced glucose uptake by tissues b. Decreased glucose uptake by tissues c. Increased insulin resistance d. Reduced insulin secretion
a. Enhanced glucose uptake by tissues
112
Which channels are blocked by sulfonylureas to stimulate insulin release? a. Sodium (Na+) channels b. ATP-sensitive potassium (K+) channels c. Calcium (Ca2+) channels d. Chloride (Cl-) channels
b. ATP-sensitive potassium (K+) channels
113
Which of the following is a first-generation sulfonylurea with the shortest action? a. Tolbutamide b. Glyburide c. Glipizide d. Glimepiride
a. Tolbutamide
114
Which generation of sulfonylurea derivatives has a longer duration of action? a. First generation b. Second generation c. Third generation d. Fourth generation
b. Second generation
115
Which second-generation sulfonylurea is considered a reasonably safe alternative to insulin therapy for diabetes in pregnancy? a. Tolbutamide b. Glyburide c. Glipizide d. Glimepiride
b. Glyburide
116
Which of the following is NOT a second-generation sulfonylurea? a. Glyburide b. Glipizide c. Tolbutamide d. Glimepiride
c. Tolbutamide
117
Which second-generation sulfonylurea is used for its longer duration of action? a. Tolbutamide b. Regular insulin c. Glimepiride d. NPH insulin
c. Glimepiride
118
What is a characteristic of second-generation sulfonylureas compared to first-generation? a. Longer duration of action b. Shorter duration of action c. Reduced efficacy d. Increased side effects
a. Longer duration of action
119
Glipizide belongs to which class of antidiabetic drugs? a. Biguanides b. Sulfonylureas c. Thiazolidinediones d. Alpha-glucosidase inhibitors
b. Sulfonylureas
120
Which sulfonylurea is recommended as a safer alternative during pregnancy? a. Glipizide b. Glimepiride c. Tolbutamide d. Glyburide
d. Glyburide
121
Which of the following is an adverse effect of sulfonylureas? a. Weight gain b. Weight loss c. Hyperglycemia d. Hyperkalemia
a. Weight gain
122
Sulfonylureas can cause which serious side effect due to excessive insulin release? a. Hyperglycemia b. Hypoglycemia c. Hypertension d. Hyperlipidemia
b. Hypoglycemia
123
Renal impairment is a particular problem in agents metabolized to: a. Inactive compounds b. Active compounds c. Neutral compounds d. Soluble compounds
b. Active compounds
124
Which sulfonylurea is particularly problematic in patients with renal impairment? a. Glipizide b. Glimepiride c. Glyburide d. Tolbutamide
c. Glyburide
125
What is a common adverse effect of sulfonylureas related to insulin action? a. Increased blood pressure b. Weight gain c. Reduced appetite d. Dehydration
b. Weight gain
126
Sulfonylureas are known to cause hypoglycemia due to their effect on: a. Decreasing insulin secretion b. Increasing insulin release c. Reducing insulin sensitivity d. Inhibiting glucose absorption
b. Increasing insulin release
127
Patients with renal impairment should be cautious with sulfonylureas that are: a. Excreted unchanged b. Metabolized to inactive compounds c. Metabolized to active compounds d. Highly protein-bound
c. Metabolized to active compounds
128
Which of the following is a less common adverse effect of sulfonylureas? a. Weight gain b. Hypoglycemia c. Hyperglycemia d. Renal impairment
c. Hyperglycemia
129
The action of meglitinide analogs is dependent on: a. Liver function b. Functioning pancreatic β cells c. Kidney function d. Muscle cells
b. Functioning pancreatic β cells
130
Meglitinide analogs bind to a distinct site on which receptor? a. Sulfonylurea receptor of ATP-sensitive K+ channels b. Insulin receptor c. Glucagon receptor d. GLUT4 receptor
a. Sulfonylurea receptor of ATP-sensitive K+ channels
131
The mechanism of action of meglitinide analogs is similar to which other class of drugs? a. Biguanides b. Thiazolidinediones c. Sulfonylureas d. Alpha-glucosidase inhibitors
c. Sulfonylureas
132
Meglitinide analogs have a rapid onset and a: a. Long duration of action b. Variable duration of action c. Short duration of action d. Intermediate duration of action
c. Short duration of action
133
Meglitinide analogs are effective in the early release of insulin that occurs: a. Before bedtime b. After a meal c. In the morning d. During exercise
b. After a meal
134
Meglitinide analogs are primarily used as: a. Fasting glucose regulators b. Postprandial glucose regulators c. Long-term glucose regulators d. Insulin sensitizers
b. Postprandial glucose regulators
135
The primary effect of meglitinide analogs is achieved by: a. Stimulating insulin release b. Inhibiting glucose absorption c. Enhancing glucose uptake d. Reducing hepatic glucose production
a. Stimulating insulin release
136
Which of the following best describes the duration of action of meglitinide analogs compared to sulfonylureas? a. Longer b. Shorter c. The same d. Variable
b. Shorter
137
Compared to sulfonylureas, the incidence of hypoglycemia with meglitinides is: a. Lower b. Higher c. The same d. Variable
a. Lower
138
Why should meglitinides not be used in combination with sulfonylureas? a. They decrease insulin sensitivity b. They increase glucose absorption c. They cause severe hypoglycemia d. They reduce the effectiveness of insulin
c. They cause severe hypoglycemia
139
Which of the following drugs is a meglitinide analog? a. Repaglinide b. Glyburide c. Glipizide d. Glimepiride
a. Repaglinide
140
Which of the following is also a meglitinide analog? a. Glimepiride b. Glipizide c. Nateglinide d. Glyburide
c. Nateglinide
141
Meglitinides should be avoided in combination with which class of drugs to prevent severe hypoglycemia? a. Sulfonylureas b. Biguanides c. Thiazolidinediones d. Alpha-glucosidase inhibitors
a. Sulfonylureas
142
Which meglitinide is included in this class of agents? a. Glyburide b. Repaglinide c. Glipizide d. Glimepiride
b. Repaglinide
143
The primary function of meglitinides is to: a. Reduce glucose absorption b. Increase hepatic glucose production c. Stimulate insulin release d. Inhibit insulin release
c. Stimulate insulin release
144
What is the benefit of using meglitinides over sulfonylureas? a. Lower risk of hypoglycemia b. Longer duration of action c. Higher potency d. Reduced side effects
a. Lower risk of hypoglycemia
145
Which of the following drugs inhibits CYP3A4 and may enhance the effect of repaglinide? a. Ketoconazole b. Rifampin c. Carbamazepine d. Barbiturates
a. Ketoconazole
146
Why must drugs that inhibit CYP3A4 be used with caution in hepatic impairment when taken with repaglinide? a. They decrease the effect of repaglinide b. They enhance the effect of repaglinide c. They have no effect on repaglinide d. They increase the clearance of repaglinide
b. They enhance the effect of repaglinide
147
Which of the following is a CYP3A4 inducer that decreases the effect of repaglinide? a. Barbiturates b. Ketoconazole c. Erythromycin d. Clarithromycin
a. Barbiturates
148
Which of the following is an effect of CYP3A4 inducers on repaglinide? a. Enhance the effect b. Decrease the effect c. No effect d. Variable effect
b. Decrease the effect
149
What is the impact of weight gain with meglitinides compared to sulfonylureas? a. It is less problematic b. It is more problematic c. It is equally problematic d. It does not occur
a. It is less problematic
150
Patients with hepatic impairment should use caution when taking repaglinide with which type of drugs? a. CYP3A4 inducers b. CYP3A4 inhibitors c. Antihypertensives d. Antihistamines
b. CYP3A4 inhibitors
151
Which antibiotic may enhance the effect of repaglinide by inhibiting CYP3A4? a. Rifampin b. Carbamazepine c. Erythromycin d. Barbiturates
c. Erythromycin
152
Compared to sulfonylureas, meglitinides are associated with: a. Less weight gain b. More weight gain c. No weight gain d. Similar weight gain
a. Less weight gain
153
The only drug member of the biguanides class is: a. Metformin b. Glyburide c. Repaglinide d. Pioglitazone
a. Metformin
154
Metformin increases glucose uptake by target tissues, thereby: a. Increasing insulin secretion b. Enhancing gluconeogenesis c. Decreasing insulin resistance d. Reducing insulin sensitivity
c. Decreasing insulin resistance
155
For its action, metformin requires: a. Glucagon b. Adrenaline c. Insulin d. Somatostatin
c. Insulin
156
Which of the following is NOT a main mechanism of action of metformin? a. Inhibiting hepatic gluconeogenesis b. Promoting insulin secretion c. Slowing intestinal absorption of sugars d. Improving peripheral glucose uptake and utilization
b. Promoting insulin secretion
157
Metformin's effects on lipid profiles include: a. Increasing LDL and VLDL b. Decreasing HDL c. Reducing LDL, VLDL, and increasing HDL d. Increasing triglycerides
c. Reducing LDL, VLDL, and increasing HDL
158
How long do the lipid profile effects of metformin typically take to manifest? a. 1-2 weeks b. 4-6 weeks c. 8-10 weeks d. 10-12 weeks
b. 4-6 weeks
159
Metformin often causes weight loss due to: a. Loss of appetite b. Increased energy expenditure c. Enhanced fat oxidation d. Decreased carbohydrate intake
a. Loss of appetite
160
Which of the following is true regarding metformin and insulin secretion? a. Metformin increases insulin secretion b. Metformin does not promote insulin secretion c. Metformin decreases insulin secretion d. Metformin has no effect on insulin secretion
b. Metformin does not promote insulin secretion
161
Metformin is recommended as the drug of choice for which condition? a. Type 2 diabetes b. Type 1 diabetes c. Gestational diabetes d. Insulinoma
a. Type 2 diabetes
162
How is metformin primarily excreted from the body? a. Metabolized by the liver b. Excreted unchanged in bile c. Excreted unchanged renally d. Metabolized by the kidneys
c. Excreted unchanged renally
163
Metformin is not metabolized in which organ? a. Kidneys b. Liver c. Lungs d. Pancreas
b. Liver
164
Metformin is effective in the treatment of polycystic ovary disease (PCOD) because it: a. Increases insulin secretion b. Reduces appetite c. Increases estrogen levels d. Lowers insulin resistance
d. Lowers insulin resistance
165
The ability of metformin to lower insulin resistance in women with PCOD can result in: a. Decreased testosterone levels b. Increased prolactin levels c. Ovulation and possibly pregnancy d. Reduced menstrual bleeding
c. Ovulation and possibly pregnancy
166
Which statement is true regarding metformin and insulin secretion? a. Metformin promotes insulin secretion b. Metformin does not promote insulin secretion c. Metformin decreases insulin secretion d. Metformin enhances insulin degradation
b. Metformin does not promote insulin secretion
167
Which of the following is a common adverse effect of metformin? a. Hypoglycemia b. Weight gain c. Gastrointestinal disturbance d. Hyperkalemia
c. Gastrointestinal disturbance
168
Metformin is contraindicated in patients with which conditions? a. Hypertension and asthma b. Renal and hepatic disease c. Hyperlipidemia and gout d. Osteoporosis and anemia
b. Renal and hepatic disease
169
Why is metformin contraindicated in renal and hepatic disease? a. It increases insulin resistance b. It increases the risk of lactic acidosis c. It reduces glucose uptake d. It promotes gluconeogenesis
b. It increases the risk of lactic acidosis
170
Which of the following conditions is a contraindication for metformin use? a. Acute myocardial infarction and congestive heart failure b. Hyperthyroidism and Addison's disease c. Rheumatoid arthritis and lupus d. Osteoarthritis and chronic bronchitis
a. Acute myocardial infarction and congestive heart failure
171
Metformin is contraindicated in patients with: a. Mild infections b. Severe infection c. Chronic allergies d. Seasonal flu
b. Severe infection
172
Metformin use is contraindicated in diabetic ketoacidosis because: a. It may exacerbate lactic acidosis b. It promotes insulin resistance c. It decreases insulin secretion d. It increases glucose absorption
a. It may exacerbate lactic acidosis
173
Long-term use of metformin may interfere with the absorption of: a. Vitamin D b. Vitamin B12 c. Vitamin K d. Vitamin C
b. Vitamin B12
174
Why is hypoglycemia less common with metformin than with sulfonylureas? a. Metformin does not promote insulin secretion b. Metformin increases insulin secretion c. Metformin decreases glucose absorption d. Metformin enhances gluconeogenesis
a. Metformin does not promote insulin secretion
175
Which of the following drugs is a member of the thiazolidinedione class? a. Pioglitazone b. Metformin c. Glyburide d. Repaglinide
a. Pioglitazone
176
Which drug is included in the thiazolidinedione class? a. Glipizide b. Metformin c. Rosiglitazone d. Nateglinide
c. Rosiglitazone
177
What is the primary mechanism of action for thiazolidinediones? a. They target the peroxisome proliferator-activated receptor (PPARγ) b. They increase insulin secretion from beta cells c. They inhibit hepatic gluconeogenesis d. They decrease glucose absorption in the intestines
a. They target the peroxisome proliferator-activated receptor (PPARγ)
178
Thiazolidinediones regulate which of the following in the body? a. Protein synthesis b. Amino acid metabolism c. Fat and glucose metabolism d. Electrolyte balance
c. Fat and glucose metabolism
179
Increased insulin sensitivity in which tissues is a result of thiazolidinedione action? a. Brain and heart b. Skin and kidneys c. Adipose tissue, liver, and skeletal muscle d. Bone and cartilage
c. Adipose tissue, liver, and skeletal muscle
180
The action of thiazolidinediones involves regulation of which receptor? a. Insulin receptor b. Glucagon receptor c. Dopamine receptor d. Peroxisome proliferator-activated receptor (PPARγ)
d. Peroxisome proliferator-activated receptor (PPARγ)
181
Thiazolidinediones do not promote which of the following? a. Glucose uptake b. Insulin secretion c. Insulin sensitivity d. Fat metabolism
b. Insulin secretion
182
Which of the following drugs does not affect LDL levels? a. Pioglitazone b. Rosiglitazone c. Metformin d. Glyburide
a. Pioglitazone
183
Rosiglitazone has been associated with an increase in which of the following? a. HDL and LDL b. LDL c. Triglycerides d. Total cholesterol
b. LDL
184
Both pioglitazone and rosiglitazone have what effect on HDL levels? a. Increase HDL levels b. Decrease HDL levels c. No effect on HDL levels d. Decrease LDL levels
a. Increase HDL levels
185
Thiazolidinediones (TZDs) lead to redistribution of fat from visceral to subcutaneous tissues, resulting in: a. Weight loss b. Weight gain c. Muscle gain d. Fat loss
b. Weight gain
186
The cardiovascular toxicity and water retention associated with which drug can lead to an increase in LDL levels? a. Pioglitazone b. Rosiglitazone c. Metformin d. Glimepiride
b. Rosiglitazone
187
Which of the following is not affected by pioglitazone? a. HDL b. VLDL c. Total cholesterol d. LDL
d. LDL
188
Which drug increases LDL levels? a. Pioglitazone b. Rosiglitazone c. Metformin d. Insulin
b. Rosiglitazone
189
What is a common effect of both pioglitazone and rosiglitazone on HDL? a. Increase in HDL levels b. Decrease in HDL levels c. No effect on HDL levels d. Variable effect on HDL levels
a. Increase in HDL levels
190
What is one of the potential adverse effects of rosiglitazone due to increased LDL? a. Hyperglycemia b. Cardiovascular toxicity c. Hypotension d. Anemia
b. Cardiovascular toxicity
191
Thiazolidinediones lead to the redistribution of fat from visceral to subcutaneous tissues, causing what side effect? a. Hypertension b. Hypoglycemia c. Weight gain d. Osteoporosis
c. Weight gain
192
Glitazones are recommended as a second-line alternative for patients who fail or have contraindications to which therapy? a. Insulin b. Metformin c. Sulfonylureas d. DPP-4 inhibitors
b. Metformin
193
How are glitazones absorbed in the body? a. Poorly from the GIT b. Well from the GIT c. Only in the presence of food d. Only when injected
b. Well from the GIT
194
Which of the following statements is true about glitazones in nursing mothers? a. Recommended for use b. Not recommended for use c. No known effects d. Required in high doses
b. Not recommended for use
195
Relief of insulin resistance by glitazones can cause ovulation to resume in which group of women? a. Postmenopausal women b. Pregnant women c. Premenopausal women with polycystic ovary syndrome d. All women
c. Premenopausal women with polycystic ovary syndrome
196
Why might women taking oral contraceptives and TZDs become pregnant? a. TZDs reduce plasma concentrations of estrogen-containing contraceptives b. TZDs increase estrogen levels c. TZDs decrease contraceptive absorption d. TZDs have no effect on contraceptives
a. TZDs reduce plasma concentrations of estrogen-containing contraceptives
197
Which of the following is not an adverse effect of glitazones? a. Hyperglycemia b. Weight increase c. Osteopenia and increased fracture risk d. Increased risk of myocardial infarction and death
a. Hyperglycemia
198
Which of the following adverse effects of glitazones occurs very rarely? a. Osteopenia b. Weight increase c. Liver toxicity d. Increased fracture risk
c. Liver toxicity
199
Which of the following is an alpha-glucosidase inhibitor? a. Acarbose b. Metformin c. Insulin d. Glipizide
a. Acarbose
200
Alpha-glucosidase inhibitors are used for the treatment of which condition? a. Type 2 diabetes b. Hypertension c. Hyperlipidemia d. Type 1 diabetes
a. Type 2 diabetes
201
When should alpha-glucosidase inhibitors be taken? a. After meals b. At the beginning of meals c. Before bed d. On an empty stomach
b. At the beginning of meals
202
How do alpha-glucosidase inhibitors work? a. By increasing insulin secretion b. By delaying the digestion of carbohydrates c. By increasing glucose absorption d. By decreasing insulin resistance
b. By delaying the digestion of carbohydrates
203
What is the mechanism of action of alpha-glucosidase inhibitors? a. Reversibly inhibiting alpha-glucosidase in the intestinal brush border b. Irreversibly inhibiting alpha-glucosidase in the liver c. Increasing pancreatic beta-cell activity d. Enhancing insulin receptor sensitivity
a. Reversibly inhibiting alpha-glucosidase in the intestinal brush border
204
Which enzyme do alpha-glucosidase inhibitors inhibit in the pancreas? a. Lipase b. Trypsin c. Alpha-amylase d. Pepsin
c. Alpha-amylase
205
Which alpha-glucosidase inhibitor is poorly absorbed? a. Acarbose b. Miglitol c. Metformin d. Glipizide
a. Acarbose
206
Which alpha-glucosidase inhibitor is very well absorbed but has no systemic effects? a. Acarbose b. Miglitol c. Metformin d. Glipizide
b. Miglitol
207
What are the major side effects of alpha-glucosidase inhibitors? a. Hypoglycemia and weight gain b. Flatulence, diarrhea, and abdominal cramping c. Hypertension and tachycardia d. Nausea and vomiting
b. Flatulence, diarrhea, and abdominal cramping
208
Why should patients with inflammatory bowel disease avoid alpha-glucosidase inhibitors? a. They can worsen colonic ulceration or intestinal obstruction b. They cause systemic toxicity c. They increase blood glucose levels d. They cause severe hypoglycemia
a. They can worsen colonic ulceration or intestinal obstruction
209
Sitagliptin inhibits which enzyme? a. DPP-IV b. Alpha-amylase c. Alpha-glucosidase d. Pepsin
a. DPP-IV
210
What is the role of DPP-IV? a. Enhances insulin secretion b. Inactivates incretin hormones such as GLP-1 c. Increases glucose absorption d. Decreases glucagon secretion
b. Inactivates incretin hormones such as GLP-1
211
How does sitagliptin affect incretin hormones? a. Prevents incretin hormone inactivation b. Decreases incretin hormone levels c. Increases glucagon levels d. Enhances insulin resistance
a. Prevents incretin hormone inactivation
212
Which of the following is a result of sitagliptin preventing incretin hormone inactivation? a. Increased insulin release in response to meals b. Decreased insulin release in response to meals c. Increased inappropriate secretion of glucagon d. Decreased insulin sensitivity
a. Increased insulin release in response to meals
213
Sitagliptin is well absorbed after which type of administration? a. Oral administration b. Intravenous administration c. Subcutaneous administration d. Intramuscular administration
a. Oral administration
214
How is the majority of sitagliptin excreted from the body? a. Through feces b. Unchanged in the urine c. Metabolized in the liver d. Through sweat
b. Unchanged in the urine
215
Dosage adjustments of sitagliptin are recommended for patients with which condition? a. Renal dysfunction b. Hepatic dysfunction c. Cardiac dysfunction d. Pulmonary dysfunction
a. Renal dysfunction
216
What are the most common adverse effects of sitagliptin? a. Nasopharyngitis and headache b. Hypoglycemia and weight gain c. Hypertension and tachycardia d. Nausea and vomiting
a. Nasopharyngitis and headache
217
The rate of hypoglycemia with sitagliptin is: a. Very low b. Moderate c. High d. Unpredictable
a. Very low
218
What is the incretin effect? a. Increased glucagon secretion with intravenous glucose b. Higher secretion of insulin with oral glucose compared to intravenous glucose c. Lower secretion of insulin with oral glucose compared to intravenous glucose d. Increased glucose absorption in the intestines
b. Higher secretion of insulin with oral glucose compared to intravenous glucose
219
Incretin effect is reduced in which condition? a. Type 1 diabetes b. Type 2 diabetes c. Hypertension d. Hyperlipidemia
b. Type 2 diabetes
220
Which of the following is an incretin mimetic? a. Exenatide b. Metformin c. Sitagliptin d. Insulin
a. Exenatide
221
What does exenatide improve? a. Glucose-dependent insulin secretion b. Insulin resistance c. Glucagon secretion d. Glucose absorption
a. Glucose-dependent insulin secretion
222
Which effect is NOT associated with exenatide? a. Slows gastric emptying time b. Decreases food intake c. Increases postprandial glucagon secretion d. Promotes beta-cell proliferation
c. Increases postprandial glucagon secretion
223
What are the consequences of exenatide administration? a. Weight gain and increased HbA1c b. Weight loss and reduced postprandial hyperglycemia c. Increased insulin resistance d. Increased glucose absorption
b. Weight loss and reduced postprandial hyperglycemia
224
How should exenatide be administered? a. Orally before meals b. Subcutaneously before meals c. Intramuscularly after meals d. Intravenously during meals
b. Subcutaneously before meals
225
What are the main adverse effects of exenatide? a. Hypoglycemia and weight gain b. Nausea, vomiting, and diarrhea c. Hypertension and tachycardia d. Nausea and headache
b. Nausea, vomiting, and diarrhea
226
Which of the following drugs is an SGLT2 inhibitor? a. Canagliflozin b. Metformin c. Sitagliptin d. Insulin
a. Canagliflozin
227
SGLT2 inhibitors are used for the treatment of which condition? a. Hypertension b. Type 2 diabetes c. Type 1 diabetes d. Hyperlipidemia
b. Type 2 diabetes
228
What is the mechanism of action of SGLT2 inhibitors? a. Increasing insulin secretion b. Decreasing glucagon secretion c. Decreasing reabsorption of glucose in the kidney d. Increasing glucose absorption in the intestines
c. Decreasing reabsorption of glucose in the kidney
229
What is the effect of inhibiting SGLT2 in the kidneys? a. Increased blood glucose b. Increased urinary glucose excretion c. Decreased urinary glucose excretion d. Increased insulin resistance
b. Increased urinary glucose excretion
230
Which adverse effect is most commonly associated with SGLT2 inhibitors? a. Hypoglycemia b. Weight gain c. Female genital mycotic infections d. Hypertension
c. Female genital mycotic infections
231
Why are SGLT2 inhibitors not indicated for the treatment of hypertension? a. They increase blood pressure b. They have no effect on blood pressure c. They are primarily indicated for glucose control d. They cause severe hypotension
c. They are primarily indicated for glucose control
232
What is an additional effect of inhibiting SGLT2? a. Increased insulin sensitivity b. Decreased reabsorption of sodium c. Increased reabsorption of potassium d. Decreased glucagon secretion
b. Decreased reabsorption of sodium
233
What is the second most common adverse effect of SGLT2 inhibitors? a. Hypoglycemia b. Urinary tract infections c. Diarrhea d. Nausea
b. Urinary tract infections